Respiratory Conditions Path Flashcards
Chronic Brochitis - Pathophysiology (7)
1) exposure to irritants and chemicals 2) inflammation 3) hypertrophy and hyperplasia of mucus secreting goblet cells 4) mucus hypersecretion 5) airway obstruction 6) alveoli hypoxia 7) decreased gas exchange
Chronic Brochitis - Pathophysiology (Blue Bloater) (5)
1) alveoli hypoxia 2) renal hypoxia 3) increased EPO secretion —> polycythaemia 4) increased renin secretion —> fluid retention 5) cyanosed and bloated
Emphysema - Risk Factors (6)
1) smoking 2) age 3) genetics (e.g. alpha-1-antitrypsin-deficiency) 4) air pollution (e.g. S2, NO2) 5) work pollution (e.g. mining) 6) Caucasian
Emphysema - Pathophysiology (8)
1) exposure to irritants and chemicals 2) inflammation 3) neutrophil elastase breaks down airway elastin 4) decreased airway elasticity 5) airway expansion on inhalation —> decreased gas exchange surface 6) airway collapse on exhalation —> airway obstruction 7) alveoli trapping 8) decreased gas exchange
Emphysema - Pathophysiology (Alpha-1-Antitrypsin-Deficiency) (3)
1) decreased hepatic production of alpha-antitrypsin 2) decreased inhibition of neutrophil elastase 3) emphysema
Emphysema - Pathophysiology (Pink Puffer) (5)
1) airway collapse on exhalation —> airway obstruction 2) exhale slowly through pursed lips 3) increased airway pressure 4) prevent airway collapse 5) flushing and puffing
Asthma - Pathophysiology (Acute Exacerbation) (14)
1) inhalation of allergen 2) allergen activates dendritic cells 3) dendritic cells attract and activate t helper 2 cells 4) t helper 2 cells activate plasma cells 5) plasma cells produce IgE 6) IgE bind to mast cells 7) allergen binds to IgE/mast cell complex 8) mast cell releases histamine 9) histamine causes 1st wave bronchoconstriction and inflammation (after minutes) 10) t helper 2 cells activate eosinophils 11) eosinophils release major basic protein 12) major basic protein induces mast cell histamine release 13) histamine causes 2nd wave of bronchoconstriction and inflammation (after hours) 14) re-inhalation of allergen recurs process
Asthma - Pathophysiology (Chronic Remodelling) (4)
1) goblet cell metaplasia —> increased mucus 2) mast cell hyperplasia —> increased histamine 3) smooth muscle hypertrophy —> airway narrowing 4) basement membrane thickening —> airway narrowing
Asthma - Pathophysiology (Asthmatic Triad) (3)
1) airway obstruction 2) airway hyperresponsiveness 3) airway inflammation
Pulmonary Embolism - Pathophysiology (3)
1) deep vein thrombosis (esp. pelvis, legs) 2) thromboembolus blocks pulmonary artery 3) v/q mismatch
Tuberculosis - Pathophysiology (Primary) (5)
1) airborne exposure to Mycobacterium tuberculosis via respiratory droplets 2) alveolar macrophages ingest M. tuberculosis 3) M. tuberculosis survive and proliferate within alveolar macrophages 4) alveolar macrophages die and release M. tuberculosis 5) asymptomatic —> flu-like symptoms
Tuberculosis - Pathophysiology (Latent) (6)
1) type IV cell mediated delayed hypersensitivity reaction to M. tuberculosis 2) subpleural caseating granuloma forms due to tissue necrosis (Ghon focus - initial granuloma) 3) M. tuberculosis spreads to hilar lymph nodes 4) lymph node caseating granuloma forms (Ghon complex - subpleural and associated lymph nodal granulomas) 5) granulomas fibrose and calcify (Ranke complex - calcified Ghon complex) 6) M. tuberculosis lies dormant
Tuberculosis - Pathophysiology (Reactivated) (5)
1) M. tuberculosis reactive due to compromised immune system (e.g. ageing, severe infection) 2) M. tuberculosis spreads throughout lungs (esp. upper lobes, more oxygenation) 3) memory immune response to M. tuberculosis 4) caseous necrosis forms lung cavities 5) M. tuberculosis disseminates throughout lungs
Tuberculosis - Pathophysiology (Miliary) (2)
1) M. tuberculosis disseminates to vasculature 2) M. tuberculosis disseminates systemically
